Time course of release of inflammatory markers after coronary stenting: comparison between bare metal stent and sirolimus-eluting stent

Background High levels of release of inflammatory markers after coronary angioplasty are predictors of late restenosis. Sirolimus-eluting stent reduces the risk of restenosis. Aim of the study To compare the release of inflammatory markers after coronary angioplasty with sirolimus-eluting stent and bare metal stent. Methods Sixteen patients with a proximal left anterior descending coronery artery stenosis were randomly assigned to receive either bare metal stent (n=8) or sirolimus-eluting stent (n=8). We measured simultaneously aortic and coronary sinus concentrations of the von Willebrand factor antigen, tumor necrosis factor-alpha and interleukin-6 before, immediately and after 2 h after stenting. High-sensitivity C-reactive protein and troponin-1 circulating levels were measured before and 6 and 24 h after coronary angioplasty. Results Before stenting, all values were similar in both groups. The coronary sinus change of the von Willebrand factor antigen level between baseline and 2 h after stenting was + 20.1 +/- 26.9% in the bare metal stent group and - 5.7 +/- 23.02% in the sirolimus-eluting stent group (P < 0.05). We observed a significant increase in the von Willebrand factor antigen (from 132.8 +/- 58.8 to 169 +/- 40.7%, P < 0.05) systemic concentrations 24 h after stenting in the bare metal stent group but not in the sirolimus-eluting stent group (from 140.6 +/- 84% to 136 +/- 39.5%), P = NS). Conclusion The present study shows that a difference in the release of inflammatory markers can be detected after coronary stenting with bare metal stent or sirolimus-eluting stent. The lower release of the von Willebrand factor antigen in the coronary sinus 2 h after the procedure and the lower systemic concentrations of the von Willebrand factor antigen 24 h after stenting in the sirolimus-eluting stent group are likely to reflect a reduced production of the von Willebrand factor antigen at the site of the vascular injury.